Zombie-Werewolf Coinfection Study

My studies have brought me near to a host of biological horrors that many have never dreamed of, much less thought to be real.

Perhaps the most notable of these studies have been pathogens:

• Human Vampiric Virus (HVV)
• Lycanthropic Parvovirus (LPV)
• Human Zombism Virus (HZV)

and others.

Each of these contagions resculpts its victim into a grotesque parody of the human form, its medium not of clay, but of bones, sinew, and flesh. Indeed, each virus is a reminder of how delicate our humanity truly is.

But individual studies of these viruses, though important, could only ever form an… incomplete picture. I knew that to truly understand them, I needed to observe and document their interactions with each other.

Now, my valued reader, I will present to you the outcome of an extended study into just what occurs when a victim of lycanthropy is exposed to the virus that leads to zombism.

Be warned: the results may not be what you expect.

Background of Study

Following my observations of specimens singularly afflicted with lycanthropy, and of those with zombism, there was still much to be discovered.

I do not have the resources I once did, but I knew that if ever these diseases were to become widespread, the possibility of a coinfection with one--or more--of these cryptic pathogens could lead to even more catastrophic effects than either could achieve on their own.

And so I set out to obtain specimens for my research.

This was more difficult than it sounds, as my studies of lycans, in particular, had previously only been the result of deceased individuals.

But even now, I do still have some… connections. After some time, a few willing participants were procured.

Now, before I proceed, I should clarify that in most cases, the mental state of those individuals affected by LPV quickly deteriorates into something animalistic.

There is no cure, nor can there be one, given the complete remodeling not only of morphological structures, but of cerebral structures as well, as a result of the viral infection.

Participants in this study were fully informed of their situation, having been exposed to the LPV in some form prior to their recruitment, and were given the choice to proceed. Their contributions to this critical research will be forever remembered.

LPV Recap

I have spoken at length regarding The Werewolf (LPV) and The Zombie (HZV) in previous recordings. However, a brief survey of these viruses is warranted for this purpose.

The Lycanthropic Parvovirus, or LPV, is a novel strain of zoonotic virus belonging to the family Parvoviridae, having specialized to infect both canines and primates. Like others of its family, LPV is a non-enveloped single-stranded DNA virus.

But in contrast to its relatives, LPV does not destroy host cells. Upon entering a cell, the viral DNA immediately integrates itself into the host's chromosomes, and new LPV virions bud from the host cell, leaving it intact, though altered.

Within a week post-infection, the victim has begun to exhibit the hallmarks of the lycanthropic appearance: widespread hypertrichosis, or hair growth, violent behavior, degradation of communication, and the early stages of an agonizing reshaping of bones and soft tissues, the latter of which many do not survive.

Those that do are entirely transformed, for lack of a better word, within about six weeks. The end result is a human stripped of their higher brain functions, primarily due to a reduction of the prefrontal cortex and hippocampus, with a pronounced mesocephalic snout, and a primarily quadrupedal form of locomotion.

Notably, and contrary to popular notions, these changes are not tied to any lunar cycle, nor can they be reversed.

HZV Recap

The Human Zombism Virus, on the other hand, works very, very differently.

It belongs to mononegavirales--the same family as those that cause rabies and ebola, as well as vampirism. Like LPV, it is zoonotic and often transmitted via bites. Unlike HPV, however, it is a negative-strand RNA virus, and utilizes a reverse transcriptase enzyme to produce DNA from its own RNA genome. This new DNA is then absorbed into the host's nucleus and incorporated into its genome via an integrase enzyme.

This effectively makes it a pro-virus, transforming the cell and directing it to synthesize new virions.

Of course, HZV's replication strategy is inherently destructive to the host cells, leading to widespread cellular damage, necrosis, and the near complete breakdown of bodily functions. This is followed by a rapid decline in the host's physiological condition, with symptoms of aggression, decay, and cognitive decline evident within mere hours.

Victims of HZV enter a comatose state approximately 1-2 hours following exposure to the virus. In this state, blood flow, respiration, metabolism, and even cardiac function are reduced to nearly nothing. Brain function is greatly affected, and in fact, the victim frequently appears deceased.

Following this phase of infection, the victim reawakens, though the heart has ceased to function entirely. Instead, skeletal muscle performs the role of blood circulation--albeit poorly. As a result, widespread organ failure and tissue necrosis is rapidly evident.

Ultimately, these two viruses employ strategies that could almost be considered opposite one another.

And this is precisely what makes this case study of… particular interest.

Coinfection

In the natural world, the concept of coinfection is not only common, at times it is thought to be more common than single infection.

In these cases, the two agents of infection often, paradoxically, compete with each other while simultaneously increasing both agents’ rate of infection by overwhelming the immune system.

In some cases, the presence of two or more pathogens can be a net positive for both, especially in terms of transmission and progression.

This is a concept known as syndemism.

But the interactions between HZV and LPV cannot be so neatly categorized.

At the cellular and biochemical level, these two viruses engage in a fierce competition for the host's cellular machinery and resources, often negatively impacting their respective pathogenic processes.

LPV, aiming to integrate and express its genetic material within the host's DNA, relies on the host's transcription and translation systems for the production of viral proteins necessary for the lycan transformation. This process demands a significant share of the host's nucleotides and energy resources, such as ATP, as well as the use of ribosomes for protein synthesis.

HZV, on the other hand, replicates its RNA genome by commandeering the host cell's ribosomal machinery to synthesize its viral proteins, a process that similarly exhausts cellular ATP and nucleotide pools.

The clash appears to arise when both viruses simultaneously attempt to utilize these cellular resources. Eventually, the host cell simply cannot adequately support the replication and protein synthesis demands of both viruses.

As I have observed first-hand, this competition can result in impaired replication for both viruses, disrupting the typical progressions of transformation and resulting in grotesquely mixed phenotypic traits.

In short, this particular coinfection is nothing short of a biological horror.

If Infection Occurs in Early Stages

Given my current lack of resources, locating a suitable environment for study proved nearly as difficult as procuring specimens for study.

But with the aid of my assistant, we eventually stumbled upon a decrepit, though large and isolated warehouse.

Observations were conducted over a period of six months. Sample size included **** individuals of roughly the same age, late twenties to mid thirties, and generally considered to have previously been in good health.

This study followed three phases, each based on the level of LPV infection in the victim and the progression of the associated symptoms.

Phase One

Phase one, as one might expect, introduced the zombie virus to a host in the very early stages of LPV infection--within 2-3 hours following an infected canine’s bite.

At this point, the LPV has begun to integrate its genetic material into the host’s DNA, but the spread of the virus has not yet reached every tissue, and the genetic changes that will result in the lycan phenotype have not yet been expressed.

At this stage, the host is usually experiencing generic symptoms, such as fever, chills, increased metabolism, etc.

The introduction of HZV at this stage disrupts LPV’s entire infection process. Due to the zombic virus’ ability to aggressively “hijack” the host’s cellular machinery for protein synthesis, it effectively monopolizes the resources necessary for both its replication and the expression of LPV-induced alterations.

In short, at earlier stages, the human zombic virus simply outcompetes the Lycanthropic Parvovirus, halting the eventual lupine transformation. Instead, the death-like coma indicative of an HZV infection will ensue, though generally delayed by several hours, and the host will “awaken” as usual.

Interestingly, however, the semi-intelligence that normally lingers for a day or so in a traditional zombie infection is absent when the host has previously been exposed to LPV. Instead, the victim will awaken with immediate and extreme aggression, and exhibit increased locomotive speed when compared to standard HZV victims at this stage.

Of course, the combination of the arrested heart and gradual systemic necrosis will take its toll as usual, and so within approximately a week, the coinfected morphology is indistinguishable from that of single HZV infection.

Phase Two

In the later stages of LPV progression, usually after roughly six weeks post-infection, the lycan transformation is largely complete, resulting in the hallmark canine-like appearance, hypertrophic musculature, and the loss of higher mental faculties.

Phase two, then, was the introduction of HZV in victims averaging 5.5 weeks following an infected LPV bite.

During this transformative phase, the increased production of growth hormones, epidermal growth factor, fibroblast growth factor, and insulin-like growth factors promote rapid cell division, muscle and bone growth, and enhanced tissue regeneration. Provided the lycan is able to feed consistently, this elevated hormonal cocktail circulates throughout the lycan’s body indefinitely.

As a result, if the Human Zombic Virus is introduced at this stage, the cellular damage it induces in its host is naturally counteracted.

In my findings, this occurs in several ways.

First, through its integration into the host genome, LPV appears to upregulate genes involved in the DNA damage response, which promotes the repair of the multiple forms of genetic damage induced by the zombic virus.

We see a clear example of this in the victims’ neural tissues. You see, generally speaking, HZV exhibits cytopathic effects on these tissues, leading to neuronal cell death. It also affects these tissues indirectly, inducing a chronic inflammatory response--the latter of which contributes to further neural damage and dysfunction.

HZV’s replication within neurons also disrupts normal cellular functions, leading to apoptosis or necrosis, and the inflammatory response exacerbates this damage, potentially leading to demyelination and loss of neural connectivity.

However, notably, the previously-mentioned elevated levels of growth factors in the LPV host actually stimulate neurogenesis and the repair of both neurons and glial cells--effectively counteracting the mental degradation caused by HZV.

Similar enhanced repair mechanisms can be observed in multiple tissue types, which serves to slow the necrotic damage induced by HZV at the systemic level.

Notably, no cardiac arrest occurs in victims at this stage, nor does any kind of coma, a hallmark of traditional HZV infection.

However, it should be noted that while the effects of the lycan virus do work to counteract many symptoms normally brought on the zombic virus, HZV infection is not so easily defeated.

The success of a lycan fending off the HZV appears to depend on multiple factors, beginning with viral load. In short, it appears that an exceptionally high concentration of HZV can overwhelm the host's cellular machinery and immune response, outpacing the regenerative processes induced by LPV altogether.

And though additional long-term studies will be necessary to confirm, it seems likely that over time, the continuous battle between LPV-induced regeneration and HZV-induced degeneration will deplete the host's resources, allowing HZV to gain the upper hand, so to speak. This possibility isn’t unique to this phase, however, and so we will return to this concept momentarily.

Physically, late-stage victims of this particular coinfection also exhibit grotesque external symptoms.

My observations consistently demonstrated that the covering of thick body hair brought on by hypertrichosis is interrupted by patches of epidermal necrosis and inflammation brought on by HZV.

Depending on the severity of HZV infection, one may also observe regions of highly decayed flesh, even exposed bone. But even these sites may exhibit reticulated scar tissue, as the enhanced healing rate brought on by LPV attempts to overcome the damage.

I have also observed that the enhanced lycan sensory abilities are often moderately reduced in these late-stage victims. Interestingly, however, olfaction may actually be improved--a noted side effect of HZV’s proliferation of olfactory receptors and limbic neurons.

Ultimately, though the LPV resists and counteracts any new infection, even one so aggressively damaging as HZV, prognosis for the late-stage host is highly dependent on initial overall health and viral load. In my testing, *** of the *** total sample size were able to resist the long-term effects of HZV effectively, exhibiting only moderate symptoms before returning to near-baseline lycan health levels.

In *** individuals, however, symptoms were more pronounced, and limited tissue necrosis, reduced cognition, and sensory impairment persisted for the duration of the study. Long-term observations will be required to accurately determine the extent of this variation, especially in relation to longevity.

But while the preceding two phases provided invaluable data, neither could prepare me fully for the… horrors… that awaited me in the third.

Phase Three

At this point, I must admit, the psychological toll of this testing was beginning to wear not only on me, but also my assistant. These are cruel diseases, and, frankly, after watching person after person descend into this madness and pain… well, continuing becomes a matter of pure will.

In any case, for this third phase of testing, we were able to obtain three additional specimens--each in the same age range as the others had been, and between 15-20 days post LPV infection.

This is a period of the most profound changes in the lycan morphology--bones are elongating, the posture becomes stooped, and the victims are in clear and near-constant discomfort as nearly every tissue in their body is being actively reshaped.

It is this stage that, upon the introduction of the Human Zombic Virus, results in the highest level of variability.

A moderate dose of HZV was given to each specimen. Approximately four hours later, two of the three specimens began to exhibit hallmark signs of infection, such as a spike in heart rate and the onset of high fever. Shortly after this, each succumbed to the typical zombic coma, wherein the heart rate slows and eventually stops, while the fever continues, escalating to the point of damaged brain function.

The third specimen exhibited a similar initial reaction, but did not fall unconscious, and in fact, appeared to “recover” fully within three hours.

Of the two that did enter the coma, one awakened within two hours, much shorter than the typical four to six. And though his heart-rate slowed significantly, interestingly, it never fully arrested.

Sadly, the other specimen did not reawaken at all and expired within approximately 57 minutes after falling unconscious. An autopsy revealed signs of severe metabolic exhaustion, such as decreased ATP production and elevated markers of oxidative stress.

Ultimately, the struggle to accommodate--and fight--the dual viral infections likely contributed to an overall weakened condition and impaired regenerative capabilities.

In terms of immune response, this unfortunate outcome is not surprising, as upon co-infection, the immune system faces two vastly different pathogens.

As previously established, LPV subtly alters host cellular functions without eliciting direct cytolysis, while HZV's replication mechanism is characterized by widespread cellular apoptosis.

In any case, it is clear that the body struggles greatly to cope with these infections, and to be honest, it is astounding that any individuals survive it at all.

Those that do show just how highly variable and volatile the nature of a mid-stage coinfection of this sort can be.

Over the following days, the remaining specimens, A and B, as I will call them, exhibited numerous additional and increasingly bizarre symptoms.

Externally, specimen A in particular began to exhibit striking asymmetry, with much of the right side of the body showing enhanced muscular development characteristic of LPV-induced anabolism, while the majority of the left side displayed muscular wasting and necrotic lesions, indicative of HZV's catabolic and cytopathic effects.

At the cellular level, this asymmetry appears to be the result of localized viral dominance, wherein LPV's integration into the host DNA in some bodily regions promotes protein synthesis and muscle fiber hypertrophy, whereas HZV's replication in other regions leads to increased proteolysis and apoptosis of muscle cells.

Additionally, the skin and fur exhibited abnormalities ranging from robust fur growth to ulcerated, necrotic patches.

Specimen B, which did not enter the zombic coma, exhibited a far less-pronounced juxtaposition--however, signs of severe cognitive decline became rapidly apparent.

In typical lycans, this transformative stage is marked by increased aggression and an apparent loss of higher reasoning largely resulting from the reduction of the prefrontal cortex. However, despite this, they often remain cunning, showing signs of “lower” intelligence, particularly in their hunting and evasion strategies.

Specimen B’s behavior, however, degraded further. He often flung himself against the walls of his containment, even to the point of personal injury, and regarded us with vicious, mindless intensity.

In truth, it was a tragic thing to watch, and it resurfaced memories of finding Alison's body, so mangled and broken.

In the specimen before us, the HZV began to degrade the senses of sight and hearing, and the characteristic lycan responsiveness was lost almost entirely--with the notable exception of smell.

Interestingly, the eyes of Specimen B exhibited a striking heterogeneity; the left eye retained the enhanced clarity typical of lycan transformation, while the right eye exhibited cloudiness and reduced responsiveness, a sign of HZV-induced cataract formation.

Within 24 hours following exposure to HZV, both specimens exhibited what appeared at first to be improved reflexes. I attributed this to the combined regenerative effects of the viruses--particularly to the increased muscular innervation caused by HZV.

However, the specimens soon exhibited overly-heightened sensitivity to stimuli, to the point that gentle prodding seemed to induce visceral reactions, as well as sporadic muscle spasms throughout the body.

It became apparent that what we were seeing was, in essence, a zombified brain barely in control of a hulk of muscle and teeth.

Particularly in specimen A, heart rate never returned to pre-coma baseline levels, and blood samples indicated increasingly viscous consistency due to raised iron and bile levels, which, in turn, reduced overall circulation.

This led, inevitably, to a continual spread of necrosis in multiple tissues, particularly of the muscle and surface dermal layers in the extremities.

However, because the heart continues to beat, unlike in single HZV infections, contractions of the skeletal muscle are not critical to circulation. In one way, this is good, because the muscular spasms in coinfected individuals appear random, uncoordinated, and somewhat violent--a far cry from the systematic, almost rhythmic pulsations seen in single infected.

Specimen B exhibited far fewer spasmodic contractions, especially as the lycan transformation progressed.

In this state of partial transformation, however, caught in limbo between two warring pathogens and in nearly constant distress, both specimens died within two weeks following coinfection. Prognosis Indeed, prognosis for organisms affected by this particular coinfection is dire, to say the least.

Even on their own, each strain greatly increases morbidity--LPV due to the immense physiological toll such a transformation takes on its host, even if they survive past that point, and HZV due to its inherently destructive nature.

Still, a traditional LPV victim may live for many years in the lycanthropic state. However, with the exception of *** of the late-stage victims, all of the specimens I observed were deceased within three months.

Interestingly, though, even for those that did not survive, death was preceded by a general period wherein the victims appeared to stabilize, perhaps having reached a kind of equilibrium between LPV’s regenerative effects and the degenerative effects of HZV.

However, it quickly became apparent that this continuous tension, compounded by the energy and resource demands of fighting off two viral infections, would simply deplete the hosts’ physiological reserves.

Going forward, one aspect of my work that will require more in-depth studies is that of transmission. Given our small sample size, which only included infected specimens, I was unable to determine whether the rate of infection increased as a result of coinfection, particularly through the preferred transmission vector of both contagions: a bite.

Of course, a coinfected individual would likely exhibit unpredictable transmission characteristics. For example: in the wild, the increased aggression and physical capabilities of a kind of lycan/zombie hybrid may make them more effective at spreading both infections.

However, the clear and visible signs of decay and the erratic behavior associated with this coinfection could make potential victims more cautious and less likely to engage with the host, potentially reducing transmission opportunities.

It also appears that the loss of cunning lower intelligence in the lycan brain makes them far less efficient hunters, and therefore less likely to be able to spread either disease.

Conclusion

By the time my study concluded, my perspective on these viruses and their effects on a host were forever altered.

Beyond the biological effects of each individual strain, the complete usurpation of the victims’ humanity is staggering. For now, their prevalence in the wild is minimal, especially in humans, and outbreaks have been swiftly contained.

But what will happen if these infections begin to overlap more frequently? I fear the result is much greater difficulty in containment. A zombified lycan, afterall, a creature whose outward appearance is a patchwork of symptoms, possesses a singular, mindless directive … to consume at any cost.